Our Research
Our lab investigates how glia and neurons coordinate to shape cognition across neurodevelopment, brain aging, and neurodegeneration. Using human stem cell–derived neural systems, rodent models, and advanced bioengineering platforms, we dissect the cell-type–specific mechanisms that drive neurological disease. Our overarching goal is to translate these mechanistic insights into precise, cell-targeted therapeutic strategies for disorders including Alzheimer’s disease and Angelman syndrome.
Astrocytes — CHI3L1/YKL-40 and the Regulation of CNS Inflammation
Defining how astrocyte-derived CHI3L1/YKL-40 drives inflammatory signaling to reveal new intervention points in AD, autoimmune demyelination, and impaired neurogenesis: we investigate how CHI3L1/YKL-40 modulates astrocyte reactivity, immune communication, and the inflammatory microenvironment across neurodegenerative and autoimmune contexts.
Microglia — KLF2, APOE, and AD-Linked Mutations in 3D Hybrid Model Systems
Illuminating how microglial regulatory pathways shape aging, neuroinflammation, and synaptic dysfunction to uncover new microglia-targeted therapeutic avenues: we study KLF2, APOE, and additional AD-relevant variants using a next-generation 3D hybrid human–rodent microglia model, enabling physiologically relevant dissection of microglial contributions to AD and brain aging.
Neurons — BIN1 Control of Endosomal and Autophagic Homeostasis
Identifying neuronal BIN1-dependent pathways that drive tau spread and vulnerability, paving the way for BIN1-based therapeutics in Alzheimer’s disease: we examine how BIN1 shapes endosomal trafficking, autophagy, and secretory dynamics, and how its disruption contributes to neuronal stress and tau pathology.
Oligodendrocytes — UBE3A-Dependent Myelination Defects in Angelman Syndrome
Revealing how UBE3A loss impairs oligodendrocyte development to inform new myelin-focused therapeutic strategies for Angelman syndrome: we investigate how UBE3A deficiency alters oligodendrocyte maturation, myelination, and circuit connectivity in this neurodevelopmental disorder.